Cardiac Action Potentials Are Extremely Long

Two major differences between action potentials in skeletal muscle and cardiac muscle have already been mentioned: First, cardiac muscle cells are electrically connected, whereas skeletal muscle cells are electrically isolated.

A third important difference between skeletal and cardiac action potentials is their duration (Figure 19-4). The entire action potential in a skeletal muscle lasts only 1 to 2 msec. A cardiac action potential lasts about 100 times longer (100-250 msec). Prolongation of the cardiac action potential is brought about by prolonged changes in the permeability of the cardiac muscle membrane to sodium (Na⁺), potassium (K⁺), and Ca²⁺ ions. Cardiac muscle cell membranes have Na* and K⁺ channels similar to those found in skeletal muscle, but the timing of their opening and closing is different in cardiac muscle. In addition, cardiac cell membranes also have special Ca²⁺ channels that are not present in skeletal muscle. The move­ment Ofextracellular Ca^2t through cardiac Ca²⁺ channels has an especially important role in prolonging the cardiac action potential. The presence of Ca^{2 4} channels and the important role of extracellular Ca²' in the action potential is the fourth major difference between cardiac and skeletal muscle.

To understand the special significance of the membrane Ca²⁺ channels in cardiac muscle, it is useful to review the roles of K⁴ and Na⁺ channels in skeletal muscle and to emphasize some ways in which cardiac K* and Na' channels are similar to those in skeletal muscle. As explained in Chapter 4, many of the K^t channels in a neuron or skeletal muscle cell membrane

FIGURE 19-4 Action potentials in cardiac muscle cells (top) last 100 times longer than action potentials in nerve or skeletal muscle cells (middle).

are open when the cell is at rest, and most of the Na¹ channels are closed. As a result, the resting cell is much more permeable to K’ than to Na'. The tendency of the positively charged K^f to leave the cell creates a resting membrane potential (polar­ization) in which the inside of the cell membrane is negative in comparison with the outside. The resting membrane poten­tial is typically between -70 and -85 mV (see Figure 19-4, bottom). An action potential is created when something depolarizes the cell (makes it less negative inside). Depolar­ization to the threshold voltage for opening the voltage-gated Na¹ channels allows an influx of extracellular Na⁴ into the cell. This rapid entry of positive ions causes the cell mem­brane to become positively charged on its inside surface. This positive membrane potential persists for only a moment, how­ever, because the Na^r channels become inactivated very quickly, and the cell rapidly repolarizes toward its resting membrane potential. Repolarization is also promoted by the opening of additional K⁺ channels. In fact, this opening of extra K⁺ chan­nels may cause neurons and skeletal muscles to become hyper­polarized (even more negative than normal) for a few moments at the end of each action potential (see Figure 19-4, bottom).

In a resting skeletal muscle cell, calcium ions are stored within the intracellular organelle called the sarcoplasmic retic­ulum. The occurrence of an action potential in the skeletal muscle cell causes Ca²* to be released from the sarcoplasmic reticulum into the free intracellular fluid, which is called the cytosol. The increase in cytosolic Ca²' concentration initiates muscle contraction (see Figure 1-5). The contraction initiated by a single action potential is very brief in skeletal muscle, because the cytosolic Ca²⁺ is rapidly pumped back into the sarcoplasmic reticulum by active transport, and the muscle relaxes. Note that the Ca²ⁱ responsible for initiating skeletal muscle contraction comes entirely from the intracellular storage site, the sarcoplasmic reticulum. No extracellular Ca²* enters the cell during the action potential, because skeletal muscle cells do not have membrane Ca²⁺ channels. In cardiac muscle, in contrast, membrane Ca²" channels and the entry of extra­cellular Ca²⁺ into the cells play key roles in both action potentials and contractions.